AEGiS-11IAC: Thrombocytopenia in pediatric AIDS patients.

11th International AIDS Conference

Vancouver, British Columbia — July 7-12, 1996

Thrombocytopenia in pediatric AIDS patients.

Int Conf AIDS 1996 Jul 7-12; 11:450 (abstract no. Pub.B.1077)
Yu CL, Della Negra M, Queiroz W, Manzoni EM, Barreto JA; Instituto de Infectologia Emilio Ribas, Sao Paulo, Brazil. Fax: +55-11-280.3954.

OBJECTIVES: To analyze the incidence, clinical evolution and therapeutic response of thrombocytopenia in Pediatric AIDS patients.

METHODS: We analyzed retrospectively the development of thrombocytopenia in a cohort of 372 HIV-infected children (CDC criteria) followed in our center from December 1986 to December 1995. The parameters studied were the incidence, clinical evolution, presence of associated infections, clinical response to therapeutic regimens with immunoglobulin, antiretroviral drug therapy or corticosteroids, as well as blood cells count (BCC) and bone marrow aspiration (BMA).

RESULTS: Twenty-seven children (6.7%) developed thrombocytopenia during the period of follow up, and could be divided in 3 different groups. The first group consisted of 10 children, in which thrombocytopenia was the first clinical manifestation of HIV infection. All of these children presented it by the development of petechiae or hematomata. None of these children presented any moderate or severe infections during the period of thrombocytopenia. Five children established a second group and presented transient asymptomatic thrombocytopenia during the evolution of HIV infection and the diagnosis could only be done by routine BCC tests. Low platelet count was the only finding in BBC tests and the BMA showed normal cellularity. The third group consisted of 12 children that presented thrombocytopenia during severe opportunistic infections or wasting syndrome, with minor or no clinical manifestations. Differently of the 2 preceding groups, BCC showed invariably low white and red cells count also, and the BMA revealed global hypocellularity. Good response to therapy was observed only among the children in the second group; the first group showed transient increase in the platelet counts, with frequent relapses.

DISCUSSION: Probably these 3 groups differ on the pathogenesis of the thrombocytopenia. We believe that the first group showed disorders of the humoral immunity, with excessive production of anti-platelet antibodies, since no other factor was found. The second group may show transient disorders of the immune system due to a possible mild infections since no relapses were observed after the initial episode. In the third group the mechanisms enrolled are probably the same described in the pathogenesis of thrombocytopenia associated to severe infections added to the medullar depletion observed in advanced stages of HIV-associated immunodeficiency. A detailed study of the clinical and immunological factors enrolled in the pathogenesis of thrombocytopenia in these patients will provide data for a better management of this disorder.

Keywords: AEGIS, Thrombocytopenia, Acquired Immunodeficiency Syndrome, Platelet Count, HIV Infections, Centers for Disease Control and Prevention (U.S.), Blood Cell Count, Incidence, Child, Human, ICA11

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